Lecture 3 Flashcards
Respiratory Viruses
Respiratory viruses are a group of viruses that primarily infect the respiratory system, which includes the nose, throat, and lungs. These viruses can cause a wide range of respiratory infections, from mild colds to severe respiratory illnesses.
Common Respiratory Viruses
Influenza Viruses (Orthomyxoviruses)
Parainfluenza Viruses (Paramyxoviruses)
Adenoviruses
Rhinoviruses (Picornavirus)
Coronoviruses
Influenza Virus
Disease: Influenza, The flu
2 day incubation period
Parainfluenza Virus
1-3 day incubation period
Laryngitis
RSV (respiratory syncytial virus)
Causes Broncioliitis
Rhinovirus
Common Cold
Corona Virus
Common Cold & SARS & Covid-19
Adenovirus
Pharyngitis
ORTHOMYXOVIRUSES:
Influenza viruses are a prominent group of orthomyxoviruses:
ORTHOMYXOVIRUSES
Orthomyxoviruses are a family of single-stranded RNA viruses that primarily infect vertebrates, including humans and various animal species.
Influenza Virus
Nose & Lower respiratory tract
Properties of the Influenza Viruses
Section title
What type of virus is an influenza virus? (RNA/DNA?)
Single Stranded RNA Negative virus
ssRNA (-)
What type of envelope do influenza viruses have?
Pleomorphic envelope that can vary in size & shape of envelope
Capsid shape of an influenza virus?
Helical nucleocapsid capsid
(cylindrical shape)
What is the genome of the influenza virus structured like?
Segmented genome
Each segment typically contains the genetic code for specific functions or proteins necessary for the virus’s replication and survival.
8 RNA (-) segments
Antigenic Shift **
Genetic structures enhance the chance of reassortment of gene segments
What can antigenic shift cause (big picture)
Mutant strains can cause epidemics, pandemics
Which strands of influenza affect humans?
Influenza A & B
What regions of the body does the influenza virus affect?
Respiratory Tract & the epithelium there
Where does transcription and replication occur?
In the nucleus
Where does assembly & release occur?
At the plasma membrane
Replication Scheme
– section title
Section title
What will ssRNA (-) be converted into?
ssRNA needs to be converted into ssRNA (+) before being able to translate into viral proteins or packaging
There are two strands created from one replication of an influenza virus. What are they?
The read (-) strand and the copy (+) strand
What happens with the read strand?
the ssRNA (-) is converted to ssRNA (+) through RNA dependent RNA polymerase
and then the ssRNA (+) is able to be used for the translation of viral proteins
What happens with the read strand?
the ssRNA (-) is converted to ssRNA (+) through RNA dependent RNA polymerase,
& RNA dependent RNA polymerase uses this strand to make a new ssRNA (-) strand to be used in packaging of the new virus of in the nucleus
The newly synthesized ssRNA(-) strands, along with other viral components, are used in the assembly of new virus particles (virions) within the host cell.
What are some influenza gene products associated with the RNA genome?
PB2, PB1, PA – complex of 3 subunits forms the RNA polymerase
NP – nucleocapsid protein
What makes up the RNA polymerase?
PB2, PB1, PA
Two surface proteins on the influenza virus
Influenza viruses have two important parts on their surface: hemagglutinin (HA) and neuraminidase (NA).
hemagglutinin (HA)
helps the virus stick to and enter host cells by binding to a molecule called sialic acid on the cell’s surface.
neuraminidase (NA)
After the virus multiplies inside the cell, it needs to get out and infect more cells.
That’s where NA comes in.
NA is like a pair of scissors that cuts the sialic acid, allowing the new virus particles to be released from the infected cell.
M2 (Membrane Protein)
M2 is a membrane protein that acts as a channel. It helps the virus by allowing the release of its genetic material inside the host cell. This is a crucial step in the virus’s life cycle, as it enables the virus to start replicating.
M1 (Matrix Protein):
M1 is a structural protein that provides stability and shape to the influenza virus. It forms a matrix beneath the viral envelope, helping to maintain the structural integrity of the virus particles.
NS1 (Non-structural Protein 1)
NS1 is an antagonist of the host’s immune system, particularly the interferon (IFN) response. It helps the virus by interfering with the host cell’s antiviral defenses. This allows the virus to replicate and spread more effectively within the host.
NS2 (Nuclear Export Protein):
NS2 plays a role in exporting viral ribonucleoprotein complexes (vRNPs) from the nucleus of the host cell
NS2 helps transport them to the cytoplasm where they can be used in the production of new viral particles.
Slide 10: Structure of an influenza virus
Ties everything together. Take a look and identify the membrane proteins, the nucleocapsid, etc.
Host range
refers to the spectrum of different host species or cell types that a particular virus can infect and replicate within. It defines the range of organisms or cells that are susceptible to infection by a specific virus.
Influenza A Host Range
Humans, swine, avian’s, marine mammals, bats
Influenza B Host range
Humans & seals
Influenza C host range
Humans & Seals
Life cycle of Influenza (VIDEO)
https://www.youtube.com/watch?v=tB5FQZi4HKY
How does an influenza virus attach to a host cell?
Hemagglutinin binds to a host receptor that has sialic acid at the end of it
How does the virus enter the cell?
Through endocytosis
Does this form a vesicle?
Yes, when a virus enters a host cell through endocytosis, a vesicle will form.
What is the role of a lysosome in the replication of a virus?
The lysosome and vesicle will fuse together and the acidity of the lysosome will be used to activate an ion channel that allows for proteins to enter the virus and start the next step of replication.
Uncoating process:
The proteins that rush into the virus detach the viral genome and allow for it to later be excreted from the cell
Hemagglutinin’s role in the release of the viral genome
Conformational change that stimulates membrane fusion (the membrane of the virus & the new membrane taken on during endocytosis)
RNA in the cytoplasm
8 segments.
NPs are on the RNA segments. Other proteins make up the RNA polymerase.
These are (-) RNA Strands and must be copied into a complementary + Strand
Cap snatching
In order to make a mRNA for translation, a 5’ cap must be added to the RNA strand. The viral RNA polymerase will cut OFF the cap of the host’s mRNA cap and helps it start replicating.
(this is crazy)
RNA & Protein Production
New RNA leaves the nucleus and goes to the cytoplasm where ribosomes will translate the Viral mRNA like envelope proteins
Nucleocapsid Proteins
Will go into the nucleus & help stabilize newly made mRNA strands
Newly made RNA Polymerase
Will go into the nucleus and make more (-) strands to serve as the RNA gene segments of new viruses.
Protein formation
Proteins are made in the nucleus & the envelope is made on the ER and go to the Golgi and then to the plasma membrane.
New Virus budding
Newly made genome, proteins and envelope are budded out of the cell
Influenza Syndrome
The virus inherently causes harm to body cells & destroys cells. The immune system’s response, however, will also lead to fever, inflammation, body aches etc.
Pneumonia
Is a less frequent outcome of the influenza disease, but if a secondary bacteria infection (due to a weakened immune system) occurs it will develop
Viral pneumonia
Influenza is one of the viruses that can lead to viral pneumonia. Influenza can weaken the immune system and damage the respiratory tract, making the body more susceptible to secondary bacterial and viral infections, including pneumonia.
Day 0-2: Exposure and Incubation
Incubation period: The virus is replicating in the respiratory tract, but the person does not yet have any symptoms.
Day 3-4: Onset of Symptoms
Symptoms of influenza begin to appear.
Prodrome: The person may start to feel mild symptoms, such as fatigue, sore throat, and a low-grade fever.
Days 5-7
Clinical disease: The person is likely to experience the most severe symptoms of influenza, such as fever, cough, sore throat, muscle aches, and fatigue.
Days 8-10
Symptoms start to improve.
Days 11-14 & Days 14-28
Recovery: Most people will have recovered from influenza by this time.
OR
Days 14-28:
Convalescence: Some people may experience fatigue and other mild symptoms for a few weeks after they recover from influenza.
Antigenic Drift
Gradual changes in influenza virus surface proteins (hemagglutinin and neuraminidase) due to mutations, leading to reduced antibody effectiveness over time.
Is a slower process.
Drift is slow, Shift is swift.
Antigenic Shift
Sudden, major changes in influenza virus surface proteins (hemagglutinin and neuraminidase) due to reassortment of genetic material, potentially leading to the emergence of new, pandemic strains.
Drift is slow, Shift is swift.
Which type of mutation can be the cause of pandemics?
Antigenic Shifts:
There have been four major antigenic shifts: in 1947, 1957, 1968, and 2009. Each of these shifts resulted in a pandemic.
Paramyxoviruses
They are enveloped, single-stranded RNA viruses that are known for their ability to infect and replicate in respiratory and mucosal tissues.
Includes:
RSV
Parainfluenza
Measles
Mumps
Parainfluenza Viruses
Parainfluenza viruses are a group of viruses that belong to the Paramyxoviridae family. These viruses are known to cause respiratory infections in humans, particularly in children. Parainfluenza viruses are a common cause of various respiratory illnesses, and there are four main types: types 1, 2, 3, and 4.
Properties of Paramyxoviruses
Section title
Section title
–
Envelope Type?
Paramyxoviruses have a variable, pleomorphic envelope surrounding them, which contains specific viral attachment proteins for host cell entry.
What type of nucleocapsid
helical or spiral shape.
Genome type
Large, ssRNA (-) Viruses
Nucleocapsid- associated proteins
Paramyxoviruses carry additional proteins associated with the nucleocapsid, which plays a role in protecting and delivering the viral genome.
What are paramyxoviruses classified by
3 genera that are distinguished by attachment proteins
What diseases can they cause
Measles, mumps & RSV
Induce syncytia formation
Paramyxoviruses have the ability to induce the fusion of infected host cells, resulting in the formation of multinucleated cells called syncytia.
How do they invade cells?
Through membrane fusion
How are they released?
Through budding
How are they transmitted?
Transmitted through aerosols & establishing infection in the respiratory tract
Morbillivirus
Measles Virus
Paramyxovirus
Mumps
Parainfluenza
Pnuemovirus:
RSV
Metapneumovirus
Replication Scheme of Paramyxoviruses
Same as influenza.
ssRNA (-) so it has to convert to positive first, read and copy strand, etc etc.
Nucleocapsid-associated proteins
NP (nucleoprotein) – binds & protects viral RNA
P (polymerase phosphoprotein) – facilitates RNA replication
L (RNA polymerase): viral replication.
F Protein (Fusion Protein)
Produced in host cell
A membrane protein that promotes fusion of the viral envelope with host cell membranes and facilitates viral entry.
HN (Hemagglutinin-Neuraminidase)
A protein that serves both hemagglutinin (binding to surface receptors) and neuraminidase functions.
Found in the Parainfluenza virus and Mumps.
G (Glycoprotein)
Functions as an attachment protein, but is not a hemagglutinin
Found in Paramyxoviruses like RSV (Pneumovirus).
M protein
Matrix Protein:
Helps with the assembly of virions
Structure of Paraxymoviruses
Slide 24 & 25
Identify the envelope, the capsid, the bilateral, the membrane protein, etc.
Life Cycle of a Paramyxovirus
Same as influenza virus except for syncytial formation
Syncytial Formation
The virus will fuse together multiple individual cells into a single, larger, multinucleated cell. This fusion results in the shared cytoplasm and nuclei of the individual cells within the syncytium.
Syncytial formation is a critical aspect of viral pathogenesis because it can lead to tissue damage, affect organ function, and contribute to the severity of viral diseases.
Measles
Inoculation -> local spread -> lymphatic spread -> viremia (virus spreading through the mode of the blood) -> spreads to the whole body -> RASH!!! -> recovery (and lifetime immunity)
Rare outcomes of measles
Encephalitis
Subacute Sclerosing Panencephalitis (rare progressive fatal disorder)
Mumps
Inoculation -> local replication -> viremia -> systemic infection, can spread to the parotid gland (swelling in the neck), the testes/ovaries nerves etc & pancreas (juvenile diabetes)
Difference between mumps and measles
Measles: RED RASH
Mumps: Swelling of neck
Adenoviruses
They are a group of double-stranded DNA viruses known for causing a variety of illnesses, from mild respiratory infections to more severe diseases
Which parts of the body are affected?
Adenoviruses can affect the respiratory tract, eyes (causing pink eye), gastrointestinal tract, lymph nodes, urinary tract, nervous system, muscles and joints, and ears, leading to various symptoms and illnesses.
Does it have an envelope?
No!!!!! No envelope
What is the shape of the capsid?
Icosadeltahedral (shape we’ve seen a million times)
Genome type (adenoviruses)
DsDNA Virus
double-stranded DNA virus
Can a DNA virus be negative or positive sense?
no pls be fr
only for RNA viruses
Genome type (linear, sequenced etc)
Linear
How many serotypes? (in adenoviruses)
52 serotyped but 1-7 are the most common
Where are adenoviruses replicated and assembled?
IN the nucleus
How does a adenovirus behave in a permissive host cell?
Will be lytic
(takes advantage of the cell) :(
How does a adenovirus behave in a non-permissive host cell?
Will be latent or persistent
(A latent infection is when the virus hides inside the host cell and can reactivate later, while a persistent infection involves ongoing viral replication in the host.)
When is a adenovirus transformative? (in what cell type)
Non human cells
Adenoviruses are extensively studied
used in RNA splicing, and in anti-viral or cancer therapy
Replication scheme of Adenovirus
DNA-dependent RNA polymerase will read and transcribe the DNA into mRNA which is then translated into viral proteins
DsDNA is copied & transcribed. What happens when its copied?
the new copy that is formed is used in packaging the new virus in the nucleus
Immediate Early Genes:
are the first to activate and play a key role in starting the infection.
Early genes
come next and help with viral DNA replication.
Late genes
are the last to activate and help create new virus particles.
Genes are activated in a certain order. Why?
Genes in viruses are activated in a specific order to ensure that the viral replication cycle is well-coordinated and efficient.
Fibers at vertices:
Adenoviruses have fiber-like structures at their corners, which help them attach to host cells.
Viral attachment proteins
Adenoviruses use these proteins to bind to host cells, ensuring a specific fit.
Type-specific antigens
These antigens give adenoviruses their unique serotypes, which is what allows them to be recognized by the immune system.
Toxic to cells (Adenoviruses)
Adenoviruses can be harmful to host cells. When adenoviruses infect a host cell, they hijack the cellular machinery to replicate themselves.
Penton Projections (Adenovirus)
Are toxic to cells
The pentons appear to be responsible for a toxic effect on cells, which manifests as clumping and detachment in vitro.
Attach via Ig Superfamily Glycoprotein
Refers to the mechanism by which certain adenoviruses attach to host cells using a receptor from the immunoglobulin superfamily of glycoproteins.
Coxsackie Adenovirus Complex
A subgroup of adenoviruses that share the Coxsackie-adenovirus receptor (CAR) for cellular entry and belong to a particular viral complex
Coxsackie-Adenovirus Recepto
An immunoglobulin superfamily glycoprotein that serves as the receptor for some adenoviruses, allowing them to attach to host cells.
Adenoviruses can also bind to MHC Class I. Why is this significant?
Some adenoviruses try to hide from the immune system by interfering with MHC class I, making it harder for the immune system to recognize and attack the infected cells.
How are adenoviruses internalized?
Receptor-Mediated Endocytosis
The process by which adenoviruses enter host cells after attaching to receptors on the cell surface, facilitating their internalization through endocytic mechanisms.
Then the vesicles it enters in is lysed and the viral genome enters the nucleus
E1A & E1B:
E1A: Adenovirus E1A proteins inhibit the function of p53 and p105RB (Retinoblastoma protein). By inhibiting these cellular proteins, E1A promotes cell cycle progression and helps the virus replicate in host cells.
E1B: E1B proteins also inhibit p53 and contribute to the regulation of cell cycle progression.
E2 (Adenovirus)
The E2 gene encodes viral DNA polymerase, which is essential for replication of the viral genome
E3 (adenovirus)
E3 proteins have various functions, including immunosuppression. They can block apoptosis (programmed cell death) and decrease the expression of major histocompatibility complex class I (MHC I) on the surface of infected cells. By reducing MHC I expression, the virus can evade immune recognition.
E4
E4 proteins also play a role in preventing apoptosis and can contribute to the overall inhibition of cell death. This helps create an environment favorable for viral replication
Viral-Associated RNAs (VA RNAs)
Help inhibit the host cell’s interferon (IFN) response. Interferons are part of the host’s innate immune response, and by inhibiting their effects, adenoviruses can counteract antiviral defenses.
L1-L5
These genes encode structural and capsid proteins that make up the viral particle. These proteins are involved in the formation of the viral capsid, which protects the viral genome and plays a role in viral attachment to host cells.
Early Genes: (adenovirus)
E1A
E1B
E2
E3
E4
Viral-Associated RNAs (VA RNAs)
These genes are among the first to be expressed when the virus infects a host cell.They are essential for manipulating the host cell cycle and interfering with the host’s defense mechanisms. They promote viral replication and help establish a favorable environment for the virus within the host cell.
Late genes
L1-L5
These genes are expressed later in the viral life cycle, typically after the early genes have already facilitated viral replication and immune evasion. The proteins encoded by these genes are primarily structural components of the virus, including the proteins that make up the viral capsid. They are necessary for the assembly of new viral particles and their release from the host cell.
Transmission of Adenoviruses
Inhalation
Close contact
Oral/Fecal roite
fomites (inanimate objects that have the pathogen)
poorly chlorinated pools
Spread Of Adenoviruses
Viermia- Blood stream
Hallmark of Infection: Adenoviruses
Inclusion Bodies Without Cellular Enlargement: A distinctive feature of the infection is the presence of inclusion bodies within cells, but these bodies do not lead to cellular enlargement.
Clinical Diseases of adenovirus
Acute febrile pharyngitis and pharyngoconjunctivital fever.
Acute respiratory disease, which can present as laryngitis, bronchiolitis, or pneumonia.
Conjunctivitis (commonly known as pink eye) and swimming pool conjunctivitis.
Gastroenteritis, which is characterized by inflammation of the stomach and intestines.
Potential sites of infection: Adenovirus
Slide 36 flow chart
Can spread from eyes to the respiratory to the gastrointestinal to the lymph nodes, viremia, skin and then either latency or resolution
Picornaviruses
Picornaviruses are a family of small, non-enveloped, positive-sense, single-stranded RNA viruses.
The name “picornavirus” is derived from “pico,” meaning small
rhinoviruses
They are small, non-enveloped, positive-sense, single-stranded RNA viruses. Rhinoviruses are well known for being one of the primary causes of the common cold in humans.
Sites of infection for picornaviruses
Picornaviruses like rhinoviruses typically infect the respiratory system causing the common cold, while other types, such as enteroviruses, can infect the gastrointestinal system and cause diseases like gastroenteritis. Some picornaviruses, like poliovirus, can also infect the nervous system, leading to conditions like poliomyelitis, and others may target specific tissues or organs.
Picornaviruses: Properties
SECTION TITLE
Enveloped? (Picornaviruses)
No!
Capsid shape (Picornaviruses)
Icosahedral Capsid
Genome type? (Picornaviruses)
ssRNA (+) Viruses
Genome structure (segmented, linear)? (Picornaviruses)
Linear mRNA genome
Where are Picornaviruses assembled?
In the cytoplasm
T/F: Picornaviruses are a large family of viruses
True
They comprise a diverse group of viruses within the Picornaviridae family, with numerous genera, species, and serotypes. Some well-known picornaviruses include rhinoviruses, enteroviruses, and hepatoviruses, which infect a wide range of hosts, including humans, animals, and plants.
T/F: Picornaviruses are not resistant to harsh conditions.
False:
Can tolerate a wide pH range
How can Picornaviruses be transmitted?
fecal-oral route
What type of virus is it? (Picornaviruses) (lytic, nonlytic, etc.)
Lytic
has specific tropisms: Viruses often have tropisms for particular host cells or tissues, which can vary between different viruses.
Replication scheme of Picornaviruses
ssRNA (+) virus is directly translated into viral proteins
Replication scheme of Picornaviruses
copy strand
RNA dependent RNA polymerase converts the + strand into a - strand : This negative-sense strand is complementary to the positive-sense RNA and serves as a template for making more positive-sense RNA strands.
The newly synthesized negative-sense RNA strand then acts as a template for the synthesis of additional positive-sense RNA strands. These new positive-sense RNA strands are used as both templates for protein synthesis and as the genetic material for new virus particles.
Enteroviruses
Poliovirus: Causes poliomyelitis (polio).
Coxsackie A virus: Associated with various diseases, including hand, foot, and mouth disease.
Coxsackie B virus: Can cause a range of illnesses, including myocarditis and pleurodynia.
Echovirus: Responsible for various infections, including aseptic meningitis.
Rhinovirus
Rhinoviruses primarily infect the upper respiratory tract and are a common cause of the common cold.
Cardiovirus
Cardioviruses, such as encephalomyocarditis virus, can infect the heart and central nervous system in animals.
Aphthovirus
Aphthoviruses, particularly foot-and-mouth disease virus, infect cloven-hoofed animals, causing a highly contagious disease.
Hepatovirus
Hepatoviruses, like hepatitis A virus, primarily infect the liver, causing hepatitis A.
What is the primary cause of the common cold?
Rhinoviruses
Rhinoviruses & ICAM1
They use ICAM-1 (Intercellular Adhesion Molecule-1) as their receptor for host cell attachment and entry.
To infect a host cell, the virus’s capsid proteins interact with ICAM-1 on the surface of the host cell.
Rhinovirus resistance
Prefer cooler temperatures
Have less resistance than enteroviruses
* they cannot tolerate the GI tract
Rhinovirus: mode of transmission
aerosols or fomites
replicates mostly in the nose
How do rhinoviruses take advantage of human cells receptors?
By binding to ICAM-1, a human cell receptor.
Rhinovirus, specifically certain strains of rhinovirus, has structural features on its capsid (the protein coat that surrounds the viral RNA) that allow it to interact with and bind to ICAM-1 (Intercellular Adhesion Molecule-1), which is a receptor on the surface of host cells.
Rhinovirus Genome Structural Protiens
Structural Proteins:
VP1, VP2, VP3, VP4: These proteins make up the viral capsid, which surrounds the RNA genome. They are responsible for protecting the viral RNA and facilitating its attachment to host cells.
Rhinovirus Genome
Nonstructural Proteins:
2A, 2B, 2C, 3A, 3B (VPg), 3C, 3D: These proteins are involved in various aspects of the viral life cycle, including viral replication and the production of new virus particles.
2A’s function specifically
the 2A protein is known for its ability to inhibit eIFs (eukaryotic initiation factors), which are essential for the initiation of protein translation in host cells.
This inhibition of eIFs is part of the virus’s strategy to disrupt the host cell’s protein synthesis machinery and redirect it for the virus’s own replication and protein production. By interfering with eIFs, the virus can reduce the host cell’s ability to make its own proteins, leading to various effects, including a weakened cell and impaired immune response
CoronaVirus
These viruses can cause a range of illnesses, from the common cold to more severe respiratory infections.
Nose & Lower respiratory tract
Coronavirus Properties
Section title
enveloped or naked? (coronavirus)
enveloped
genome structure (corona virus)
long, flexible, helical genome
genome type (corona virus)
ssRNA (+)
Glycoprotiens on coronavirus surface
crown-like appearance, hence the name “coronaviruses.”
Corona: GI Tract Resistance
The crown-like projections, or “corona,” provide resistance to the acidic environment of the gastrointestinal (GI) tract, allowing the virus to survive in the digestive system.
Upper Respiratory Tract Infection: corona
Coronaviruses primarily infect the epithelial cells of the upper respiratory tract, leading to respiratory symptoms.
How is coronavirus released?
Through exocytosis
Optimal temperature for growth?
33°C and 35°C.
What’s the second most common cause of the common cold?
corona virus
SARS
Certain coronaviruses, such as SARS (Severe Acute Respiratory Syndrome), MERS (Middle East Respiratory Syndrome), and COVID-19 (caused by SARS-CoV-2), can lead to severe and potentially life-threatening respiratory diseases.
Replication scheme: corona virus
Same as the other ssRNA (+) schemes
Structure of corona virus
Slide 49
Point out crown projections,
capsid, the envelope , etc
Coronavirus Life cycle
nothing new here
Gene Products of corona virus
section title
section title
L - RNA polymerase
This protein is responsible for viral RNA replication and transcription, playing a key role in the reproduction of the virus’s genetic material.
HE (Hemagglutinin-Esterase):
This protein is found in some viruses, including certain coronaviruses. It can have functions related to receptor binding and esterase activity, aiding in the virus’s attachment to and entry into host cells.
S (Spike or Attachment Protein):
The spike protein is often a crucial component of a virus’s structure, particularly in coronaviruses. It plays a role in attaching to host cell receptors and facilitating viral entry.
E (Envelope Protein):
The envelope protein is involved in the formation and maintenance of the viral envelope, which surrounds the viral particle. It is essential for the structure and stability of the virus.
M (Matrix Protein):
The matrix protein provides structural support for the viral envelope and helps determine the shape of the virus particle.
N (Nucleocapsid or RNA-Binding Protein):
The nucleocapsid protein binds to the viral RNA, protecting it and assisting in its replication and packaging.
SARS CoV-2
The spike protein of SARS-CoV-2, the virus responsible for COVID-19, contains an RBD that binds to the angiotensin-converting enzyme 2 (ACE2) receptor on the surface of human cells. This binding is essential for the virus to enter and infect the host cell.
How does SARS-CoV-2 Virus attach to human cells
- Spike Protein and ACE2: The spike protein of SARS-CoV-2 has a three-lobed structure with extensions. These extensions are initially folded down. The virus needs to bind to the ACE2 receptor on the surface of human cells to enter and infect the cell.
- Protease Cleavage: Before the virus can bind to ACE2, a protease enzyme comes in and cuts the spike protein. This “cut” allows the spike protein to open up, similar to a flower blooming.
- Binding to ACE2: Once the spike protein is in its open and extended form, it can bind to the ACE2 receptor on human cells. This binding is like a key fitting into a lock and is necessary for the virus to enter the host cell.
- Activation in Human Cells: Importantly, this activation step, which involves the protease cleavage and binding to the ACE2 receptor, is specific to human cells. It allows the virus to gain entry into human cells but does not occur in cells from other species.
